Antecedent systemic inflammation has recently been demonstrated to be associated with an increased risk of incident type 2 diabetes. This is manifest as elevations in fibrinogen increased while blood cell count, decreased serum albumin and elevations in certain coagulation factors including factor VIII. Our new findings demonstrate that among non- diabetics, periodontal disease is associated with impaired fasting glucose (IFG) but not impaired glucose tolerance (IGT), suggesting that periodontitis may contribute to the metabolic abnormalities seen in this one subset of pre-diabetic subjects. To further examine this relationship we propose to conduct a randomized, no-treatment controlled, study in 96 subjects with IFG and 96 with IGT to determine where periodontal therapy reduces clinical biomarkers of poor metabolic control fasting glucose, fasting insulin and C-peptide), acute phase reactants in serum (C-reactive protein and IL-6) and oxidative stress (serum 8-iso PGF/2alpha). These changes will be determined treating half of the subjects in each group with scaling and root planing and measuring each of these biomarkers at 6 weeks, 3, 6,9 and 12 months. The remaining half of the patients will serve as delayed treatment controls and will be treated at exit. We expect to see a lowering of fasting blood glucose levels in response to periodontal treatment indicating that periodontal infection contributes to the metabolic dysfunction seen in pre-diabetes. If proved this may represent a new primary intervention strategy to prevent new cases of type 2 diabetes.